2 research outputs found
Sensory and cognitive mechanisms of change detection in the context of speech
The aim of this study was to dissociate the contributions of memory-based (cognitive) and adaptation-based (sensory) mechanisms underlying deviance detection in the context of natural speech. Twenty healthy right-handed native speakers of English participated in an event-related design scan in which natural speech stimuli, /de:/ (“deh”) and /deI/ (“day”); (/te:/ (“teh”) and /teI/ (“tay”) served as standards and deviants within functional magnetic resonance imaging event-related “oddball” paradigm designed to elicit the mismatch negativity component. Thus, “oddball” blocks could involve either a word deviant (“day”) resulting in a “word advantage” effect, or a non-word deviant (“deh” or “tay”). We utilized an experimental protocol controlling for refractoriness similar to that used previously when deviance detection was studied in the context of tones. Results showed that the cognitive and sensory mechanisms of deviance detection were located in the anterior and posterior auditory cortices, respectively, as was previously found in the context of tones. The cognitive effect, that was most robust for the word deviant, diminished in the “oddball” condition. In addition, the results indicated that the lexical status of the speech stimulus interacts with acoustic factors exerting a top-down modulation of the extent to which novel sounds gain access to the subject’s awareness through memory-based processes. Thus, the more salient the deviant stimulus is the more likely it is to be released from the effects of adaptation exerted by the posterior auditory cortex
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Reduced brain serotonin transporter availability in major depression as measured by [ 123I]-2β-carbomethoxy-3β-(4-iodophenyl)tropane and single photon emission computed tomography
Background: Prior research has suggested reductions in the density of serotonin transporter (SERT) binding sites in blood platelets and post-mortem brain tissue of depressed patients. We sought to determine whether patients with unipolar major depression have diminished SERT availability as assessed by both brainstem [
123I]β-CIT SPECT and platelet [
3H]paroxetine binding.
Methods: Drug-free depressed and healthy subjects were injected with 211 ± 22 MBq [
123I]β-CIT and imaged 24 ± 2 h later under equilibrium conditions. A ratio of specific to nonspecific brain uptake (V
3″ = (brainstem-occipital)/occipital), a measure proportional to the binding potential (B
max/K
d), was used for all comparisons.
Results: Results showed a statistically significant reduction in brainstem V
3″ values in depressed as compared to healthy subjects (3.1 ± .9 vs. 3.8 ± .8, p = .02). Platelet [
3H]paroxetine binding was not altered (B
max = 2389 ± 484 vs. 2415 ± 538 fmol/mg protein,
p = .91) and was not significantly correlated with brainstem [
123I]β-CIT binding (
r = −0.14,
p = .48).
Conclusions: These data are the first to suggest reductions in the density of brain SERT binding sites in living depressed patients. These findings provide further support for a preeminent role for alterations in serotonergic neurons in the pathophysiology of depression